Disruption of mCry2 restores circadian rhythmicity in mPer2 mutant mice

Henrik Oster, Akira Yasui, Gijsbertus T.J. Van Der Horst, Urs Albrecht

    Research output: Contribution to journalArticle

    101 Citations (Scopus)

    Abstract

    Many biochemical, physiological, and behavioral processes display daily rhythms generated by an internal timekeeping mechanism referred to as the circadian clock. The core oscillator driving this clock is located in the ventral part of the hypothalamus, the so called suprachiasmatic nuclei (SCN). At the molecular level, this oscillator is thought to be composed of interlocking autoregulatory feedback loops involving a set of clock genes. Among the components driving the mammalian circadian clock are the Period 1 and 2 (mPer1 and mPer2) and Cryptochrome 1 and 2 (mCry1 and mCry2) genes. A mutation in the mPer2 gene leads to a gradual loss of circadian rhythmicity in mice kept in constant darkness (DD). Here we show that inactivation of the mCry2 gene in mPer2 mutant mice restores circadian rhythmicity and normal clock gene expression patterns. Thus, mCry2 can act as a nonallelic suppressor of mPer2, which points to direct or indirect interactions of PER2 and CRY2 proteins. In marked contrast, inactivation of mCry1 in mPer2 mutant mice does not restore circadian rhythmicity but instead results in complete behavioral arrhythmicity in DD, indicating different effects of mCry1 and mCry2 in the clock mechanism.

    Original languageEnglish
    Pages (from-to)2633-2638
    Number of pages6
    JournalGenes and Development
    Volume16
    Issue number20
    DOIs
    Publication statusPublished - 2002 Oct 15

    Keywords

    • Circadian clock
    • Cry
    • Nonallelic suppressor
    • Per

    ASJC Scopus subject areas

    • Genetics
    • Developmental Biology

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  • Cite this

    Oster, H., Yasui, A., Van Der Horst, G. T. J., & Albrecht, U. (2002). Disruption of mCry2 restores circadian rhythmicity in mPer2 mutant mice. Genes and Development, 16(20), 2633-2638. https://doi.org/10.1101/gad.233702